BACKGROUND
Type 2 diabetes (T2D) is associated with an increased risk of premature death. Diet may influence long-term health outcomes among individuals with T2D, but prospective evidence on dietary patterns and mortality remains limited.
OBJECTIVES
To prospectively examine associations of eleven pre-defined or empirically-developed dietary patterns with all-cause and cause-specific mortality (e.g., cardiovascular disease [CVD] and cancer) among U.S. individuals with T2D.
METHODS
We included 7,795 participants with incident T2D in the Nurses' Health Study (1984-2016) and Health Professionals Follow-Up Study (1986-2020), who were free of CVD and cancer at diagnosis. Diet was assessed using a validated food frequency questionnaire and updated every four years. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% CIs.
RESULTS
Over 24 years of follow-up, 3,509 deaths were confirmed, including 1,079 from CVD and 649 from cancer. Adherence to healthy dietary patterns after diagnosis (comparing the 90th with the 10th percentile of dietary pattern scores) was consistently associated with lower all-cause mortality, with multivariable-adjusted HRs ranging from 0.78 (95% CI: 0.71, 0.85) for the Planetary Health Diet to 0.92 (95% CI: 0.84, 1.01) for the Dietary Approaches to Stop Hypertension. Furthermore, greater improvements in dietary pattern adherence from pre- to post-diagnosis (comparing the 90th with the 10th percentile of change scores) were also associated with lower all-cause mortality, with HRs (95% CI) ranging from 0.63 (0.58, 0.70) to 0.92 (0.85, 1.01). A similar pattern of inverse associations with CVD mortality was also observed for these dietary scores. Additionally, the reversed Empirical Dietary Index for Hyperinsulinemia was specifically associated with lower cancer mortality.
CONCLUSIONS
Adherence to healthy dietary patterns is universally associated with better survival in individuals with T2D. These findings suggest the importance of consuming high-quality diets in the prevention of premature deaths among individuals with T2D.
Zixin Qiu, Gang Liu, Binkai Liu et al.· American Journal of Clinical...· 0 citations
BACKGROUND
Peripheral artery disease (PAD) risk varies substantially across glycemic states, but glycemic status-specific proteomic features of PAD remain poorly characterized. This study aimed to provide comprehensive proteomic insights into PAD risk across the glycemic spectrum.
METHODS
We included 43,875 UK Biobank participants, categorized into normoglycemia, prediabetes, and type 2 diabetes (T2D). Associations between 2920 plasma proteins and PAD were assessed using Cox regression models. PAD-related proteins underwent pathway enrichment and protein-protein interaction (PPI) analyses, and protein predictors were selected via least absolute shrinkage and selection operator models. The differential expression-sliding window analysis identified proteomic changes across the glycemic continuum.
RESULTS
We identified 558 proteins associated with PAD risks, and those proteins were predominantly involved in pathways related to immune system regulation, inflammatory processes, and vascular remodeling. Two major PPI networks were identified, centered on tumor necrosis factor in normoglycemic participants and T-cell surface glycoprotein CD4 in those with T2D. The integration of protein predictors or derived protein risk scores into the clinical model significantly improved PAD prediction performance, achieving a maximum C-index of 0.834. Two proteomic peaks were revealed at glycated hemoglobin levels of 37 and 42 mmol/mol (5.5% and 6.0%), at which 11 and 4 proteins, respectively, showed potential causal associations with PAD.
CONCLUSION
This study revealed glycemic state-specific proteomic features of PAD risk. These findings suggest the involvement of innate immunity in normoglycemia, and adaptive immune dysregulation with chronic inflammation in T2D. Integrating proteomic data also improved PAD risk prediction. Further validation is warranted.
Hancheng Yu, Jijuan Zhang, Frank Qian et al.· Metabolism: Clinical and Exp...· 0 citations
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